'What's really exciting is that behind Gleevec came two more buses -- this one (Sutent), and a second drug. These drugs have lifted everybody's expectations all over again, for cancer in general.'

The pill, Sutent, is one of the first in a new class of cancer drugs that target multiple tumor activities at once. Doctors are hopeful the drugs will usher in a new era where combinations of finely targeted drugs can dramatically improve the prognosis of cancer patients in a similar way that triple-combination therapy has revolutionized HIV treatment.

Conventional chemotherapy drugs kill cancer cells, but they also damage healthy tissue. The newer generation of drugs specifically targets tumor cells and leave the rest of the body alone. However, those drugs target a single tumor function, don't work for everybody and can stop working after a while.

Sutent, or sunitinib malate, seems to shrink tumors by simultaneously starving them of blood, blocking signals that tell them to grow and spread and causing cancer cells to die. It is being tested in patients for whom the latest targeted drugs have failed and has shown promise in previous studies in kidney and breast cancer patients. It is one of more than 10 multitasking drugs being studied in various types of cancer.

Delayed the Time to Progression

The latest research, presented Thursday at the European Cancer Conference in Paris, studied Sutent in 312 people in Europe, the United States, Australia and Asia with a type of cancer called gastrointestinal stromal tumor, or GIST.

The prognosis of this cancer had been dire for many years, until the targeted drug Gleevec, or imatinib, came along about five years ago.

However, Gleevec stops working for most patients within two years as the tumor develops resistance to it, just like bacteria become immune to antibiotics.

In the study, two-thirds of the patients, who had all developed resistance to Gleevec, got the new drug, while one third got a fake treatment.

The medicine delayed the time to progression of the tumor from 6.4 weeks to 27.3 weeks, the study found. It is too early in the study to tell whether the treatment is saving lives.

The study was paid for by Sutent's developer, Pfizer.

'Huge Scientific Implications'

The findings are good news for GIST patients, said Dr. Gordon McVie of the European Institute of Oncology in Milan, Italy.

"There was a fear when imatinib was so successful that when resistance occurred, that was going to be it," said McVie, who was not connected with the research. "What's really exciting is that behind Gleevec came two more buses -- this one, and a second drug. These drugs have lifted everybody's expectations all over again, for cancer in general."

"We've now got two other options to offer. Each of the two drugs, sinutinib and the (as yet unnamed) Bristol Myers Squibb drug are both producing better than 50 percent remission rates all over again in Gleevec resistance, and that's fantastic," McVie said. "What's going to be very tempting as soon as these two new drugs show their spurs is to go into combination therapy with Gleevec up front."

But experts agree the promise of Sutent and other such drugs goes beyond GIST, which is being used as a proving ground for other cancers because scientists understand its simple circuitry well.

"It has huge scientific implications, that's for sure," said Dr. Jose Baselga, a medical oncologist at the Valla d'Hebron Hospital in Barcelona Spain who was not tied to the research.

Rulebook on Cancer

The study's leader, Dr. George Demetri, associate professor of medicine at the Dana Farber Cancer Institute in Boston, Massachusetts, said the findings will help scientists think more creatively about more complicated cancers.

"We are trying to put together the rulebook on cancer," he said.

The experience with HIV therapy, where huge leaps in survival were not seen until triple combination cocktails came along, has provided good lessons for cancer, Demetri said. Testing of Sutent in combination with other drugs is already under way, he said.

"The cells probably have a rather limited repertoire of tricks they can fall back on. If you put pressure on one pathway, the cell finds a different pathway to squeeze around. But if you block that pathway too, the cell is stuck. They get trapped, they can't grow and they die," Demetri said. "That's the theory."